Influence of cytochalasin D-induced changes in cell shape on proteoglycan synthesis by cultured articular chondrocytes.
Influence of cytochalasin D-induced changes in cell shape on proteoglycan synthesis by cultured articular chondrocytes.
复制标题
细胞松弛素 D 诱导的细胞形状变化对培养的关节软骨细胞蛋白多糖合成的影响。
DOI：
10.1016/0014-4827(88)90391-6
复制
发表时间：
1988
影响因子：
3.7
通讯作者：
F. Watt
中科院分区：
文献类型：
--
作者：
P. Newman;F. Watt
越来越多的证据表明，细胞形状调节多种细胞类型中的增殖和分化基因表达。我们已经探索了关节软骨细胞的形态培养和蛋白多糖的合成量和类型之间的关系，使用细胞松弛素D诱导可逆的细胞变圆。当软骨细胞被阻止伸展或伸展细胞被诱导成圆形时，35 SO 4掺入蛋白多糖被刺激。掺入到细胞层中比掺入到培养基中更受刺激。当去除细胞松弛素D使细胞重新扩散时，蛋白多糖合成恢复到对照水平。细胞松弛素D诱导的35 S 04掺入的刺激反映了核心蛋白合成的增加，而不是糖胺聚糖链的延长，因为[3 H]丝氨酸掺入核心蛋白也受到刺激。所观察到的蛋白聚糖合成的刺激不是由于蛋白质合成的整体刺激、DNA合成的抑制或细胞在细胞周期的一个阶段中的积累。细胞松弛素D处理悬浮液中的细胞没有进一步刺激35 S 04掺入，表明观察到的效应是由于细胞变圆而不是暴露于细胞松弛素D本身;然而，我们不能完全排除药物的其他非特异性效应。成纤维细胞和软骨细胞，已通过刺激去分化没有纳入更多的35 SO 4细胞松弛素D处理时，这表明，增加蛋白多糖的合成，在响应舍入本身可能是一个分化的软骨细胞的属性。
There is growing evidence that cell shape regulates both proliferation and differentiated gene expression in a variety of cell types. We have explored the relationship between the morphology of articular chondrocytes in culture and the amount and type of proteoglycan they synthesize, using cytochalasin D to induce reversible cell rounding. When chondrocytes were prevented from spreading or when spread cells were induced to round up,35SO4incorporation into proteoglycan was stimulated. Incorporation into the cell layer was stimulated more than into the medium. When the cells were allowed to respread by removing cytochalasin D, proteoglycan synthesis returned to control levels. Cytochalasin D-induced stimulation of35S04incorporation reflected an increase in core protein synthesis rather than lengthening of glycosaminoglycan chains, because [3H]serine incorporation into core protein was also stimulated. The observed stimulation of proteoglycan synthesis was not due to an overall stimulation of protein synthesis, to inhibition of DNA synthesis, or to accumulation of cells in one phase of the cell cycle. Cytochalasin D-treatment of cells in suspension caused no further stimulation of35S04incorporation, suggesting that the observed effects were due to cell rounding rather than exposure to cytochalasin D per se; nevertheless, we cannot completely rule out other, nonspecific, effects of the drug. Fibroblasts and chondrocytes that had been passaged to stimulate dedifferentiation did not incorporate more35SO4when treated with cytochalasin D, suggesting that increased proteoglycan synthesis in response to rounding may itself be a differentiated property of chondrocytes.